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Source Naturals methylb12 was the absolutely worst methylb12 and had zero activity. It was tye only zero star brand we found. The two 5 star brands are Jarrow and Enzymatic therapy. 1mg and 5mg will all be at least 1000 tiomes better than any size Source Naturals.


Freddd, At Phoenix Rising, I believe you said the “red dot” methylB12 was a zero star brand. The manufacturer of the “red dot”, “No Shot” microlingual brand of methylB12 is Superior Source. Is there any possibility you are confusing the name Superior Source with Source Naturals? If not, then is it possible you found 2 zero star brands?

Susinn says

I have a parietal cell antibody which has in the past resulted in macrocytic anemia from vitB12 deficiency. Do you know if parietal cell antibody is associated with other gut issues such as leaky gut or gut/brain axis issues? Do you have suggestions how to approach this other than sublingual B12 and folic acid?


First, don’t take folic acid – take tetrahydrofolate (natural folate). They have a different effect on the body, and some studies show increased cancer risk with folic acid. Second, you have to address the immune dysregulation, which is the underlying problem. That’s an involved process.


I am in NC. I need to dig out the recent blood tests. I am not sure if folate was part of it. I know that the doctor checked my potassium because my legs and arms hurt so badly, especially at night. She was concerned that I was having a side affect to the B12 injections. But it was fine. I need to see what was looked at on the blood panel that was ran.

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Jan, I’ll lay it out for you. I have terrible spasms and a whole lot else from low potassium starfting at 4.3, which on the scale from 3.5-5.0 is mid-scale. On the scale from 4.0-5.0 it isn’t low either. Lot’s of people start at 4.2-4.3. Further pain, not pain from spasms, can be casue d by folatye insufficiency or paradoxical folate deficiency. Start titrating methylfolate until the pain is relieved. Thsi would be a far more general and inflammatory pain than potassium. Also, IBS, cracking skin around the fingertips, sores at the corners of the mouth, allergies, asthma, MCS, nausea, and so on might flair with low folate. Most need betrween 1600 and 15,000mcg to get rid of all folate deficiency symptoms depending upon how they react to folic acid and veggetable folate. The only kind of b12 likely to do you well is methylb12 and adenosylb12. There are 3 brands of Dibencozide (adensoylb12), one with folic acid. There are two 5 star brands of methylb12, Jarrow and Enzymatoic Therapythat produce more reliable results than injections. These will make potassium drop rapidly most likely becasue healing starts immeditatly and potassium drops by the 3rd day whern that happens.


mary ann says

Figure 3.

Epithelial properties of second heart field (SHF) cells. A , Immunofluorescence of transverse sections at the level indicated by the box in Womens Carson 2 Terrain Multisport Outdoor Shoes Beige Puma nwdpE
, showing that the SHF is an atypical epithelium composed of cells with apically restricted N-cadherin and E-cadherin containing adherens junctions (arrows), a discontinuous basal lamina (arrowhead) and distinct apical and basolateral membrane domains labeled by aPKCζ and Scribble, respectively. Note the lateral accumulation of E-cadherin and continuous basal lamina in epithelial cells in overlying pharyngeal endoderm (End). B , The basolateral membrane of SHF cells in the dorsal pericardial wall (DPW) is characterized by -dependent filopodial protrusions (arrows) enriched in filamentous actin labeled with Phalloidin (red) or Utrophin-GFP (green fluorescent protein; green). The typical features and morphology of SHF epithelial cells as shown in the bottom right panel. Scale bars: A, 20 µm; B, 10 µm. A indicates apical; and B, basal. Adapted from Francou et al with permission. Copyright ©2014, The Company of Biologists Ltd.

Dynamic Filopodia and Insights Into the Regulation of Cell Biology by Tbx1

The dynamic properties of basal filopodia in murine SHF cells in the dorsal pericardial wall were explored using time-lapse confocal imaging of thick slice cultures of mouse embryos, revealing that the filopodia are highly dynamic and contact underlying mesenchymal cells, neighboring cells in the epithelium as well as ventral foregut endoderm ( Convertible charm in sterling silver with Tiffany Blue enamel finish Tiffany amp; Co imJzrA
). Filopodia have been proposed to mediate long-distance signaling during vertebrate morphogenesis, such as, for example, Hedgehog signaling in avian limb mesenchyme. Signaling filopodia have also been observed on the basal side of epithelial cells in avian somites where they have been associated with retrograde transport of the receptor Fzd7 and deposition of fibronectin and Hedgehog signaling. Whether basal filopodia play a role in transducing intercellular signaling events in the SHF remains to be determined; however, they are enriched in phosphotyrosine, consistent with activation of membrane receptor tyrosine kinases. Alternatively, basal filopodia in the SHF may be involved in cell movement into or out of the epithelium. Indeed, intercalation of expressing mesenchymal cells may contribute to growth of the epithelium in the posterior region of the dorsal pericardial wall, as will be discussed in detail below. On the other hand, basal filopodia may indicate cell movement out of the epithelium into underlying mesenchyme where cells may adopt noncardiac fates, for example, contributing to endothelium of the pharyngeal vasculature. Localized EMT of coelomic somatic mesoderm has been shown to generate mesenchyme at the onset of limb outgrowth. Filopodia may also be involved in cell movement during epithelial sheet migration through dynamic focal adhesions with the extracellular matrix and underlying endoderm, a process that has been implicated in epithelial tube formation in . Finally, basal protrusions in differentiated cells in the OFT are required for the process of myocardialization that generates the muscular outlet septum, and basal filopodia in the dorsal pericardial wall could potentially prefigure this activity. Further dynamic imaging and functional studies are necessary to resolve these questions.

Observation of null embryos revealed that loss of Tbx1 severely impairs filopodia formation and also reduces the basolateral membrane domain of SHF cells, increasing the circularity of cells in the dorsal pericardial wall ( Figure 3B ). Among the epithelial proteins analyzed, only aPKCζ was quantitatively modified in mutant embryos, being upregulated and losing its apical localization. As an apical determinant, upregulation of aPKCζ could contribute to the reduction of the basal domain of mutant SHF cells, with a concomitant deregulation of basal domain-dependent signaling. In support of this model, embryo culture in the presence of a physiological activator of aPKCζ phenocopied the epithelial defects seen in null embryos, leading to increased circularity and reduced filopodia in SHF cells; furthermore, aPKCζ activator–treated embryos showed decreased proliferation and ectopic differentiation in the dorsal pericardial wall and a shortened OFT. This is consistent with a signaling role for basal filopodia in regulating proliferation and differentiation in the SHF. Moreover, these results suggest that the regulation of the epithelial properties of SHF cells by Tbx1 may be a primary role of this transcription factor in heart development. In support of this conclusion, recent genome-wide identification of loci regulated by Tbx1 and histone 3 lysine 4 monomethylation identified pathways involved in cell morphology, adhesion, and regulation of the actin cytoskeleton, rather than those directly involved in cell proliferation and differentiation. In additional support of a role for Tbx1 in regulating cell shape, zebrafish has been shown to modulate cardiomyocyte cell shape during looping morphogenesis, through regulating the expression of genes encoding the noncanonical Wnt ligand Wnt11 and adhesion molecule alcama. Together these data point to the regulation of basic cell biological mechanisms underlying Tbx1 function in the SHF with important implications for the origin of 22q11.2 deletion syndrome patient phenotypes. Detailed characterization of Tbx1 target genes in the SHF, including identification of the mechanisms by which Tbx1 regulates aPKCζ activity, will be required to further explore this. The extent to which other transcriptional regulators of SHF development similarly control the epithelial features of these progenitor cells remains to be determined. Candidates include Hand2, which controls apicobasal polarity of cardiac progenitor cells in the zebrafish embryo and is required in the murine SHF for progenitor cell survival. SHF cell survival is also compromised, and is downregulated in embryos lacking the transcription factors Msx1 and Msx2, leading to a spectrum of OFT CHD.

Signaling Pathways and the Epithelial SHF Niche

Progressive SHF deployment is orchestrated by intercellular signaling events, including autocrine signaling and signal exchange with surrounding pharyngeal ectodermal and endodermal epithelia and neural crest-derived mesenchyme. Signaling pathways implicated in SHF development include Wnt, Notch, FGF, BMP, Hedgehog, retinoic acid, and noncanonical (β-catenin independent) Wnt pathways (reviewed in ). Epithelial properties of SHF cells, such as filopodia with a potential signaling role, are likely to be important in determining the SHF progenitor cell niche during heart tube extension. Primary cilia also play major roles in signal transduction and have been implicated as a cause of CHD. In particular, cilia are required to establish embryonic laterality pathways that direct cardiac looping morphogenesis. Primary cilia are observed on the apical surface of SHF cells and in other cell types during heart development, including valve mesenchyme and endocardium; their potential role in the SHF remains to be investigated, for example, by conditional loss of function of regulators of ciliogenesis.

Cell–cell adhesion has been implicated in defining the SHF progenitor cell niche. N-cadherin–deficient embryos have defects in myocardial growth and adhesion and fail to fully elongate the heart tube. Soh et al inactivated N-cadherin in the SHF using conditional mutagenesis and observed that the resulting embryos had a hypoplastic OFT and right ventricle. This was associated with decreased proliferation and elevated differentiation in the SHF. Loss of N-cadherin led to a reduction in cellular β-catenin levels and a decrease in components of the canonical Wnt signaling pathway, a major driver of proliferation in the SHF; by conditionally restoring β-catenin signaling, the authors could partially rescue the mutant phenotype. N-cadherin is also required for heart development in the zebrafish; mutation of N-cadherin in the mutant results in morphological and differentiation defects and altered myocardial cell shape, although a specific requirement in SHF cells has not been described. Adherens junction proteins have been shown to regulate progenitor cells in other tissues. For example, E-cadherin, also expressed in the anterior dorsal pericardial wall, is regulated by FGF signaling in the mouse incisor where it both maintains the dental stem cell niche and promotes collective epithelial cell migration; interestingly, this process is dependent. In additional support of a role for adhesion-mediated interactions in SHF development, Zeng and Yelon have demonstrated that the cell adhesion molecule Cadm4 restricts the size of the zebrafish OFT downstream of FGF signaling, by regulating the size of the progenitor cell pool. Together these results highlight the importance of cell adhesion in the SHF for both signal transduction and maintenance of the progenitor cell niche.

PCP proteins have been implicated in OFT CHD, including alignment defects such as double outlet right ventricle, although the underlying mechanisms have remained unclear. Two PCP proteins, Vangl2 and Prickle1, have recently been shown to be required for normal establishment of cell polarity in the transition zone as SHF cells differentiate at the arterial pole of the heart ( Womens Regular Dress Love Moschino nUof7L4
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In the case of Vangl2 , conditional gene inactivation in the SHF using Isl1-Cre resulted in a shortened OFT at midgestation and double outlet right ventricle at fetal stages. 56 Detailed analysis of epithelial properties in the transition zone at earlier stages revealed disruption of cell polarity, including mislocalization of N-cadherin, E-cadherin, and Scribble, together with loss of apical enrichment of aPKCζ and an expanded basolateral domain. These changes suggest perturbation of both apicobasal and planar polarity in the transition zone. Abnormal positioning of cells within the plane of the epithelium and epithelial thickening is likely to cause the OFT shortening and alignment defects in SHF conditional Vangl2 mutant embryos ( Iris amp; Ink Woman Marley Oneshoulder Ruffled Poplin Top White Size 12 IRIS amp; INK UaD2AMD
). 56 These changes were accompanied by precocious activation of differentiation markers in the transition zone suggesting early loss of the progenitor cell phenotype, further illustrating the importance of epithelial architecture in controlling SHF cell differentiation. Similarly, a missense mutation in the gene encoding the PCP protein Prickle1 in the Beetlejuice mutant mouse leads to a shortened OFT and consequent alignment defects. 90 Again, aPKCζ localization was disrupted, associated with a thickened epithelium in the transition zone. The small GTPase Rac1 has been implicated in apicobasal and PCP pathways and the regulation of cytoskeletal dynamics; conditional loss of function in the SHF has shown that Rac1 is required for maximal proliferation and epithelial organization in the SHF, including apical localization of aPKCζ, as well as OFT lengthening and alignment. 91 Interestingly, in polarized neural progenitor cells, apical aPKCζ has been shown to negatively regulate the activity of the cyclin-dependent kinase inhibitor p27, thus promoting proliferation and blocking differentiation. 92 Whether this mechanism underpins PCP OFT phenotypes remains to be seen. Together, these phenotypes highlight the importance of PCP in maintaining epithelial architecture in the transition zone.

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